| Project/Area Number |
26460270
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
WAKAYAMA TOMOHIKO 熊本大学, 大学院生命科学研究部, 教授 (70305100)
YAMAMOTO MIYUKI 金沢大学, 医学系, 助教 (60139780)
NAKATA HIROKI 金沢大学, 医学系, 講師 (80638304)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 細胞分化 / 組織形成 / 顎下腺 / 導管系 / アンドロゲン / 甲状腺ホルモン / 受容体 / カルパイン / セルピン / カリクレイン / マウス / 性差 / 顆粒性導管 / マウス顎下腺 / 生後発達 / ケラチン5 / カルパイン3 |
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| Outline of Final Research Achievements |
Of the two kinds of sexual dimorphism in the mouse submandibular gland (SMG), the preferential increase of granular convoluted tubule (GCT) cells in males was lacking in androgen receptor (AR)-deficient mice (ARKO) and, thus, proved to be dependent on AR, whereas the administration of thyroid hormone (T4) to ARKO caused increase of GCT cells independent of AR. On the other hand, the preferential decrease of granular intercalated duct (GID) cells in males was lacking in ARKO, and administration of T4 caused no decrease of GID cells, suggesting that the two kinds of sexual dimorphism have different hormone dependency. Furthermore, the gene expression profile of the normal and ARKO SMG identified numbers of new GCT-specific gene products.
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